创伤性脑损伤大鼠皮质神经元中Lnx1表达及参与继发性脑损伤的机制  

Lnx1 expression in cortical neurons of rats with traumatic brain injury and mechanisms involved in secondary brain injury

作　　者：马艳霞 杨严伟[1] 马宇航 李迪 王晓燕[5] 邹明明 韦善文 Ma Yanxia;Yang Yanwei;Ma Yuhang;Li Di;Wang Xiaoyan;Zou Mingming;Wei Shanwen(Department of Orthopedics,First Affiliated Hospital of Soochow University,Suzhou 215000,Jiangsu Province,China;Orthopedic Institute,Soochow University,Suzhou 215006,Jiangsu Province,China;Second Affiliated Hospital of Soochow University,Suzhou 215004,Jiangsu Province,China;First People’s Hospital of Zhangjiagang Affiliated to Soochow University,Zhangjiagang 215600,Jiangsu Province,China;Quality Control Department,Lanzhou Institute of Biological Products Co.,Ltd.,Lanzhou 730046,Gansu Province,China;Department of Neurosurgery,First Medical Center of Chinese PLA General Hospital,Beijing 100853,China)

机构地区：[1]苏州大学附属第一医院骨科,江苏省苏州市215000 [2]苏州大学骨科研究所,江苏省苏州市215006 [3]苏州大学附属第二医院,江苏省苏州市215004 [4]苏州大学附属张家港市第一人民医院,江苏省张家港市215600 [5]兰州生物制品研究所有限责任公司质量鉴定室,甘肃省兰州市730046 [6]解放军总医院第一医学中心神经外科医学部,北京市100853

出　　处：《中国组织工程研究》2025年第1期24-30,共7页Chinese Journal of Tissue Engineering Research

基　　金：国家自然科学基金青年项目(8180052062),项目负责人:李迪。

摘　　要：背景:细胞凋亡在继发性脑损伤中发挥重要作用。探究创伤性脑损伤后促进神经细胞存活的病理生理机制,将为防治创伤性脑损伤提供新的方向和理论依据。目的:探究Lnx1分子在哺乳动物脑损伤后皮质神经元中的表达变化及参与继发性脑损伤的可能机制。方法:80只成年SD大鼠平均分成假手术组和创伤性脑损伤组,每组雌雄各20只。采用重物坠落方法建立创伤性脑损伤大鼠模型,分别在脑损伤后6,12,24,48,72 h,通过RT-qPCR、Western blot和免疫荧光染色等技术分析相关分子在受损皮质神经元中的表达情况。结果与结论:(1)创伤性脑损伤组大鼠损伤部位脑组织出血,可观察到明显的组织损伤,脑组织含水量升高;(2)与假手术组相比,创伤性脑损伤组皮质神经元中Lnx1表达在损伤24 h开始显著升高;(3)创伤性脑损伤后与Lnx1相结合的PBK和BCR蛋白表达降低,促存活因子ctgf的表达升高;(4)结果表明:脑损伤后神经元中Lnx1表达上调,其通过降低靶分子PBK和BCR的表达,进一步上调促成活因子ctgf的表达,对受损神经元具有保护作用。BACKGROUND:Apoptosis plays an important role in secondary brain injury.Therefore,to explore the pathophysiological mechanism of promoting nerve cell survival after traumatic brain injury provides a new direction and theoretical basis for the prevention and treatment of traumatic brain injury.OBJECTIVE:To explore the expression changes of Lnx1 molecule in mammalian cortical neurons after brain injury and the possible mechanism involved in secondary brain injury.METHODS:Eighty adult SD rats were divided into 20 male and 20 female mice in sham operation group and 20 male and 20 female mice in traumatic brain injury group.The traumatic brain injury rat model was established by heavy falling method.At 6,12,24,48,and 72 hours after brain injury,the expression of related molecules in damaged cortical neurons was analyzed by RT-qPCR,western blot assay,and immunofluorescence staining.RESULTS AND CONCLUSION:(1) The brain tissue of traumatic brain injury group was bleeding and obvious tissue injury could be observed.Water content of brain tissue increased after traumatic brain injury.(2) Compared with the sham operation group,the expression of Lnx1 in cortical neurons after traumatic brain injury increased significantly at 24 hours after injury.(3) After traumatic brain injury,the expression of PBK and BCR protein decreased,and the prosurvival factor ctgf increased.(4) These findings suggest that after traumatic brain injury,the expression of Lnx1 is up-regulated in neurons,which may be due to the decrease of the expression of its target molecules PBK and BCR,and further promote the expression of living factor ctgf,which has a protective effect on the damaged neurons.

关 键 词：创伤性脑损伤 继发性脑损伤 神经元 SD大鼠 Lnx1 PBK BCR CTGF 

分 类 号：R459.9[医药卫生—治疗学] R318[医药卫生—临床医学] Q189[生物学—神经生物学]